This chemically induced mutation of the seizure threshold 2 (Szt2) gene displays an low threshold for kindling induced seizures and may be useful in the studies of seizure susceptibility.
Wayne Frankel, JAX
Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any electroencephalograhic, neurosensory or motor abnormalities. Although mice do not exhibit spontaneous seizures, non-invasive kindling produces an earlier latency to first minimal clonic seizure than C57BL/6J controls (4 tests vs. 7-8 tests). This mutant mouse strain may be useful in studies of epilepsy susceptibility.
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
This mutation was generated by ethylnitrosourea (ENU) mutagenesis in C57BL/6J males. Descendants of the mutagenized males were selected for low electroconvulsive (seizure) threshold (ECT). A point mutation (T to A) in the exon 32 splice site donor results in inclusion of intron 32. Mice were backcrossed to 129S1/SvImJ for ten generations before cryopreservation in 2010.
|Allele Name||mutation 1, Wayne N Frankel|
|Allele Type||Chemically induced (ENU)|
|Gene Symbol and Name||Szt2, seizure threshold 2|
|Strain of Origin||C57BL/6J|
|Molecular Note||A T to A mutation was induced by ENU in the exon 32 splice site donor resulting in inclusion of intron 32 in the mutant transcript. Northern blot analysis indicates about a 4 fold increase in mRNA expression in whole brains from homozygous mice.|